(HAGL) LESIONS

12
Diagnosis and Treatment of
Humeral Avulsion of the
Glenohumeral Ligament
(HAGL) Lesions
Richard K.N. Ryu / John M. Tokish
Introduction
Anterior shoulder instability continues to be among the most common cause of
disability in any young population. Failure of the inferior glenohumeral ligament
(IGHL) attachment has long been considered the “essential” lesion in this condition (1), and biomechanical studies have revealed this failure as an avulsion
occurring most commonly on the glenoid side of the joint (2). Numerous clinical studies have confirmed the intra-articular pathology associated with anterior
shoulder dislocations and have identified the Bankart lesion as nearly ubiquitous
in its association with shoulder instability (3–5). That said, humeral avulsion of
the glenohumeral ligament (HAGL), although uncommon, can be an alternative
pathologic entity contributing to shoulder instability. Failure to recognize and
address this pathology can lead to persistence of instability even after operative
intervention (6–8).
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146 Section 2 Anterior Instability
Anatomy
Stability of the shoulder joint relies upon a complex
interplay of static and dynamic stabilizers. An example
of this is found in the concavity-compression phenomenon which relies upon an intact labrum to deepen the
humeral head–glenoid interface while the rotator cuff
musculature provides the dynamic compression component. Loss of integrity of either static or dynamic
function increases the risk of instability (9).
The IGHL, the major static stabilizer, relies on an
anterior and a posterior band with an axillary pouch
suspended by the two main condensations within the
IGHL, with attachments spanning the 2- to 4-o’clock
position anteriorly, and the 7- to 9-o’clock position posteriorly. The attachment of the IGHL on the humeral
neck has been described by Pouliart and Gagey (10) as
“V” shaped, originating inferior to both the lesser and
greater tuberosities (11). The function of the IGHL has
been position dependent, and at 90 degrees of abduction combined with external rotation, the IGHL stabilizes anterior–inferior excursion of the glenohumeral
joint (12,13). Similar stability is provided by the posterior band of the IGHL when the shoulder is flexed and
internally rotated.
Pathoanatomy
Several studies have investigated the failure characteristics
of the IGHL under load. Stefko et al. (14) studied these
characteristics in a cadaveric model with the arm positioned in the abducted, externally rotated position. The
authors found that the IGHL strain increased over 7% at
failure, and that this failure occurred on the glenoid side
in 92% of cases, consistent with clinical observations of
the predominance of a Bankart lesion. Another study,
however, found that the failure mode was less consistent.
Bigliani et al. (2) demonstrated a mixed mode of ­failure
in their experimentally created model, with failure at the
glenoid attachment in 40%, midcapsular failure in 35%,
and humeral avulsion in 25%. It should be noted that the
strain rate in this study was quite low, and other authors
have suggested that the rate of loading may play a role in
the site of failure of the IGHL. Ticker et al. (11) demonstrated that mechanical failure on the humeral side (an
experimentally created HAGL) decreased to 8% when
strain rates were increased toward physiologic speeds,
lending a pathophysiologic justification to the HAGL
mechanism, and offering an explanation as to why it is
infrequently seen in the clinical setting.
Clinical investigations have cited a HAGL incidence
rate ranging from 1.5% to 9% (7,15,16) (Figs. 12-1 and
12-2). Although these lesions are encountered more
often in anterior instability cases, posterior humeral
LWBK1284-ch12_p145-154.indd 146
HH
IGHL
▲ Figure 12-1: Viewing from anterior-superior portal of a left
shoulder, ­classic appearance of HAGL lesion (arrows) with detachment from the humeral side (HH, humeral head; IGHL, inferior
glenohumeral ­ligament).
a­ vulsions of the glenohumeral ligament have been
reported as well (15,17,18). Incidence of anterior versus
posterior HAGL lesions is felt to be approximately 93%
to 7% (15) (Fig. 12-3).
It is also important to note that the HAGL lesion
does not have to occur in isolation. Warner and Beim
(19) and Field et al. (20) independently reported on the
“floating” HAGL in which a Bankart lesion is found in
combination with a HAGL lesion. This phenomenon
can best be explained on the basis of the evidence of
Speer et al. (21). Although creation of a Bankart lesion
leads to instability, capsular deformation must accompany the Bankart lesion in order for functional instability to occur. The simultaneous HAGL lesion in conjunction with a Bankart lesion may simply represent a
variation of capsular failure. An alternative explanation
HH
SSc
▲ Figure 12-2: Viewing from posterior portal of a left shoulder, a massive HAGL lesion involving much of the anterior inferior
glenohumeral ligament is visualized (arrows depict leading edge of
the HAGL lesion) (SSc, subscapularis; HH, humeral head).
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Chapter 12 Diagnosis and Treatment of Humeral Avulsion of the Glenohumeral Ligament (HAGL) Lesions
147
HH
IS
AP
PHAGL
C
▲ Figure 12-4: Viewing from an posterior–inferior portal of
a right shoulder, an axillary pouch HAGL lesion (arrows) is identified
(HH, humeral head; IGHL, inferior glenohumeral ligament).
▲ Figure 12-3: Viewing from the anterior-superior portal of
a left shoulder, a posterior HAGL lesion is noted with the avulsed
edge (arrows) clearly separated from the humeral head (HH) attachment site (AP, axillary pouch; C, cannula; IS, infraspinatus; PHAGL,
posterior humeral avulsion of the glenohumeral ligament).
of the “floating” HAGL lesion may represent a metachronous phenomenon is which one lesion occurs after
the first predisposes to continuing instability episodes
or may simply represent a failure pattern related to the
trauma experienced.
Furthermore, although commonly thought to occur
in isolation, several studies have reported on a significant rate of associated injuries. Bokor et al. (7) described
a 17% incidence of associated pathology while Neviaser
et al. (22) reported on 37 cases of anterior dislocation
with a high incidence of a subscapularis tear in combination with a humeral avulsion of the IGHL. This ­pattern
of associated pathology is echoed with posterior HAGL
lesions as well, with Castagna et al. (18) noting 66% of
their posterior HAGL lesions occurring in conjunction
with other significant shoulder pathology.
Classification
Six HAGL lesion types were originally included in
the West Point classification (15): (1) anterior HAGL,
(2) anterior bony HAGL (BHAGL), (3) posterior or
reverse HAGL (RHAGL), (4) posterior bony HAGL,
(5) anterior “floating” HAGL lesions with detachment
at both the glenoid and humeral attachments, and
(6) posterior “floating” HAGL lesions with detachment
at both the glenoid and humeral attachments. A seventh type of HAGL lesion has recently been described to
involve the axillary pouch (APHAGL) (Fig. 12-4), and
was postulated to result from repetitive microtrauma
and failure of the inferior capsule in female volleyball
players (23).
LWBK1284-ch12_p145-154.indd 147
Mechanism of Injury
Most instability episodes occur in lesser degrees of
abduction and external rotation, often requiring a powerful translation as the major deforming force. Although
no clearly proven injury pattern has been identified
that is unique to a HAGL lesion, Nicola proposed pure
hyperabduction and maximum external rotation as the
­common mechanism for the HAGL lesion (8). The activities reported to have the highest incidence of HAGL
lesions may be skewed on the basis of the prevalence of
a particular sport; however, in the largest series, rugby
was the most common pursuit, with ice hockey and
wrestling (15), motocross (24,25), skiing and ­volleyball
also described (7,24,25).
Taljanovic et al. (23) have postulated a specific
injury pattern in female volleyball players leading to an
APHAGL (axillary pouch HAGL) lesion. They proposed
that the volleyball spike requires a higher release point,
leading to greater abduction and external rotation to
achieve such a posture. Repetitive hitting in this position
leads to failure of the inferior capsule on a microtraumatic basis manifested by symptoms of pain and dysfunction rather than the typical complaints of shoulder
instability.
History and Physical Examination
Patients with HAGL lesions present with complaints
similar to other patients with instability, and special athletic populations such as rugby or volleyball, should alert
the examiner to the possibility of a HAGL phenomenon.
Patients with a HAGL lesion can complain of significantly greater instability episodes with regard to duration
and intensity and a crescendo pattern is not uncommon.
George et al. (26) reported that anterior shoulder pain
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148 Section 2 Anterior Instability
was more severe in those with HAGL lesions, and furthermore that those patients who had failed a prior stabilization procedure should be carefully scrutinized for a
HAGL lesion (7,27).
On physical examination, there is no specific finding that is pathognomonic for a HAGL lesion. The typical findings associated with shoulder instability are often
elicited during the physical examination. The principles of
inspection, palpation, range of motion, and special testing remain cogent for all patients suspected of instability.
In terms of specific testing, the apprehension test (28) is
perhaps the most accurate test for anterior instability. It
is performed either seated or supine, and the examiner
takes the patient’s arm into maximal external rotation
with the shoulder at 90 degrees of abduction. Reproduction of the patient’s symptoms is a reliable indicator of
anterior instability (29). Another method of assessment
for instability is the anterior load and shift test. This test is
performed with the patient either seated or in the supine
position and can also be undertaken with the patient in
the lateral decubitus position. This latter position is helpful as the scapula can be controlled with one hand while
the humerus is translated with the other. The humeral
head is loaded axially to ensure it is centered, and then
translated forward. The test is graded on the basis of how
far the humeral head travels in relation to the glenoid
(30): Grade 0, little movement of the humeral head;
grade 1, the humeral head rides up to the glenoid labrum;
grade 2, the humeral head is shifted off the glenoid but
spontaneously reduces when pressure is removed; and
grade 3, the humeral head is shifted off the glenoid and
remains dislocated once the pressure is removed.
For posterior instability, a similar load and shift
maneuver can be performed. A modification of this test,
the push–pull test (31), can be effective in reproducing
symptoms with posterior translation. This test is performed with the patient supine, and the arm is placed at
90-degree abduction in neutral rotation and 30-degree
horizontal adduction. The examiner grasps around the
patient’s wrist with one hand (the pull), and posteriorly
loads the humerus (the push). This places a fulcrum
on the shoulder and enhances the examiner’s ability to
control subluxation. Finally, ligamentous laxity should be
evaluated with the use of Beighton and Horan criteria (32).
A prominent sulcus sign may indicate symptomatic
multidirectional instability.
Diagnostic Imaging
Rarely do routine radiographs reveal any diagnostic evidence regarding the actual capsular injury itself
although secondary findings such as an associated
Hill-Sachs lesion or glenoid bone loss can be detected.
In the infrequent occurrence of a bony HAGL lesion,
LWBK1284-ch12_p145-154.indd 148
RC
HH
G
▲ Figure 12-5: Coronal MR image with contrast revealing
“J” sign (arrow) with avulsion of the humeral attachment of the
inferior glenohumeral ligament (HH, humeral head; G, glenoid;
RC, rotator cuff).
plain radiographs may detect the avulsed medial bony
humeral fragment adjacent to the attachment site of the
IGHL, inferior to the lesser tuberosity anteriorly and to
the greater tuberosity in posterior-based lesions. Scalloping along the medial neck of the humerus may also
be an indication of a humeral-sided failure of the IGHL.
Bokor et al. (7) noted that 7 of 41 documented HAGL
lesions were detected on plain radiographs using the
criteria described above. Because of overlapping bone
on plain x-rays, these avulsions can be easily missed on
routine films.
The imaging technique of choice when evaluating
a potential HAGL lesion is the MR arthrogram (26) in
which the typical finding confirming the HAGL lesion
is the conversion of the “U” shaped inferior capsule
into the “J” sign caused by the loss of integrity of the
IGHL humeral attachment, best seen on the coronal
view (Fig. 12-5). Extravasation of contrast on both the
sagittal oblique and the coronal view (Fig. 12-6) also
confirms the loss of IGHL integrity inferiorly.
Numerous authors have described the MR arthrographic findings, and the correlation between these findings and arthroscopic documentation has been robust
(33,34). One report warned against the “over-reading”
of MR arthrograms in the assessment of HAGL lesions.
Melvin et al. (35) described four cases in which an MR
arthrogram established a HAGL lesion by the criteria
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Chapter 12 Diagnosis and Treatment of Humeral Avulsion of the Glenohumeral Ligament (HAGL) Lesions
Ac
HH
▲ Figure 12-6: Sagittal oblique image of the avulsed inferior
capsular attachment with gross extravasation of contrast material
(arrows) (HH, humeral head; Ac, acromion).
described, and at arthroscopy although inferior capsular
pathology was noted, a detectable HAGL lesion was not
confirmed. As with most lesions that are difficult to verify with diagnostic testing or from the physical examination, arthroscopic confirmation remains the gold standard prior to treatment being rendered.
Treatment Alternatives
Patients with symptomatic HAGL lesions present similarly to other patients with instability, and decisions
regarding nonoperative versus operative management
mirror those discussions. While it is unknown whether
the HAGL lesion represents a different prognosis than
the labral avulsion with regard to risk of recurrence, progression of bone loss, or risk for late arthritis, the pathology of the acute HAGL is much clearer than its chronic
counterpart, and early intervention may be ­considered.
Delayed presentation may result in ineffective scar that
spans the gap to the humerus creating a functionally
lengthened complex with inferior biomechanical properties compared to the native ligament. This scar can be
indistinguishable from normal IGHL, and may make
the surgery more technically difficult. We prefer an early
approach to these lesions, especially in the young athlete or active laborer, as the anatomy is clearer and the
repair is histologically more sound.
LWBK1284-ch12_p145-154.indd 149
149
The surgical approach to the HAGL lesion is
directed towards a primary repair of the capsular disruption. It is critical to determine the extent of this
avulsion, as the severity of the disruption may determine the best surgical approach. For the anterior HAGL
lesion, an anatomic repair can be accomplished either
arthroscopically or through a mini-open anterior incision. Studies using both techniques have uniformly
demonstrated satisfactory outcomes with regard to
low recurrence rates and return to high-functioning
levels (16,19,20,23,36,37). The open approach, which
should always be preceded by a diagnostic evaluation
to confirm the ligament tear and associated pathology,
is achieved through a mini-incision through an axillary
approach. Arciero and ­Mazzocca (36) and later Bhatia
et al. (37) have described exposure through the inferior one-third of the subscapularis attachment, either
via an “L” shaped takedown or upward retraction of
the inferior subscapularis in the “sparing” technique
described by Bhatia. The anterior HAGL lesion is easily identified with this approach although care must
be taken not to obscure the tear by cutting through the
subscapularis and the capsule at the same time, leaving
in doubt whether the capsular defect was pathologic or
iatrogenic in nature.
When utilizing an open approach in those cases
with an associated glenohumeral ligament injury on
the glenoid side, greater exposure will be required in
order to view the glenoid attachment of the IGHL from
the lateral aspect of the joint. Once the glenoid lesion
is repaired, the humeral avulsion is repaired utilizing
a suture anchor technique with closure and shifting of
­tissue to restore capsular integrity (20).
Arthroscopic repair of the anterior HAGL lesion is
challenging. A perpendicular approach to the humeral
head is often unavailable for anchor or instrument
insertion due to the neurovascular structures inferiorly. Several techniques have been described, all of
which require advanced arthroscopic skills. Wolf et al.
(16) described an arthroscopic technique in which
sutures were passed through the HAGL lesion which was
then reapproximated to the humeral attachment site as
the sutures were brought out via an accessory anterolateral portal and tied over the deltoid fascia. Richards and
Burkhart (25) and later Kon et al. (24) were some of the
first to pioneer an all-arthroscopic technique in which
the sutures were passed and tied within the joint, using
a 5-o’clock portal through the subscapularis. In his technique, Burkhart described suture passage through the
HAGL lesion from a posterior approach while viewing
from the anterior-superior portal.
When choosing an arthroscopic repair for an
anterior–inferior HAGL lesion, visualization is of paramount importance. Using both the 30- and 70-degree
lenses through multiple portals is mandatory for this
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150 Section 2 Anterior Instability
GU
HH
PIGHL
▲ Figure 12-7:
Viewing from the anterior of a right shoulder
portal, an inferior axillary HAGL lesion is identified (arrows).
▲ Figure 12-10: Viewing from an anterior portal, a drill
guide (GU) is seen at the inferior humeral head attachment site,
facilitating transhumeral head drilling, beginning at the posterolateral aspect of the greater tuberosity (HH, humeral head; drill
pin (large arrows); APHAGL lesion (small arrows); AIGHL, anterior
inferior glenohumeral ligament).
HH
SH
PIGHL
GP
GP
AIGHL
HH
▲ Figure 12-8: Viewing from an anterior of a right shoulder
portal, the humeral attachment is prepared with a shaving tool (SH)
through a low anterior–inferior portal (arrows outline HAGL lesion)
(HH, humeral head; AIGHL, anterior inferior glenohumeral ligament; PIGHL, posterior inferior glenohumeral ligament).
▲ Figure 12-11: Viewing from a lateral subacromial portal,
two guide pins (GP) are placed through the humeral head into the
inferior aspect of the humeral head (HH).
GP
GP
▲ Figure 12-9: Viewing from a low posterior portal, the
prepared bony bed (large arrows) at the humeral attachment site
is clearly visualized (small arrows outline axillary pouch HAGL
lesion).
LWBK1284-ch12_p145-154.indd 150
▲ Figure 12-12: Viewing from a low posterior portal, the
two guide pins are seen exiting the prepared bony bed on the
humeral neck (arrows outline the sutures passed through the HAGL
lesion; GP, transhumeral head guide pins).
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Chapter 12 Diagnosis and Treatment of Humeral Avulsion of the Glenohumeral Ligament (HAGL) Lesions
151
HH
AIGHL
PIGHL
G
▲ Figure 12-13: Sutures passed through the HAGL lesion
are in turn passed through the drill tunnels and tied over a bone
bridge in the subacromial space, reapproximating the inferior glenohumeral ligament to the humeral attachment site (arrows outline
sutures passed through transhumeral head tunnels and tied in the
subacromial space).
▲ Figure 12-14: Intra-articular view of the inferior HAGL
lesion after reapproximation of the HAGL lesion to the humeral
neck (HH, humeral head; G, glenoid; AIGHL, anterior inferior glenohumeral ligament; PIGHL, posterior inferior glenohumeral ligament).
demanding procedure. The primary steps involve creating a bony trough at the humeral attachment site for
the IGHL, creating a working portal through the intra-­
articular tendinous portion of the subscapularis and
passing sutures through the HAGL lesion using either a
suture shuttling technique or a direct pass and retrieve
maneuver. In those situations in which a Bankart lesion
is encountered in addition to the HAGL lesion, the
HAGL lesion is addressed first, followed by a standard
suture anchor Bankart repair, making sure not to overtension the final construct. It is critical to appreciate the
inferior extent of the HAGL, as significant extension
makes an all-arthroscopic approach through anterior
portals potentially unsafe.
A recent surgical technique described by Taljanovic
et al. (23) addresses this challenge by approaching distal fixation through a transhumeral head technique
in which multiple sutures are passed through the free
edge of the avulsed edge of the HAGL lesion and then
brought through multiple bone tunnels drilled through
the humeral head with the use of a guided ­system. The
sutures are then tied over bone bridges along the posterior aspect of the greater tuberosity (Figs. 12-7–12-14).
The treatment of the posterior HAGL lesion is
almost always approachable from an arthroscopic
perspective. Although extracapsular repairs can also
be accomplished, intra-articular anchor placement,
suture passage and knot tying are relatively easier and
more accessible. Much like the anterior HAGL lesion,
arthroscopic treatment of the reverse HAGL lesion has
been uniformly successful (17,18,38,39). If an open
procedure is selected for posterior repair, we prefer a
deltoid split in line with its fibers, followed by dissection between the infraspinatus and the teres minor to
approach the posterior capsule. The capsular avulsion
can be identified through this interval, and repaired
back after biologic preparation with suture anchors.
This technique has been reported uncommonly, but
with successful results (40,41).
LWBK1284-ch12_p145-154.indd 151
Postoperative Rehabilitation
The principles of postoperative rehabilitation after
HAGL repair are protection with mobilization. The
patient leaves the operating room in a sling, and this
is worn full time, except during specific rehabilitative
sessions, for 3 weeks. Range of motion limitations are
dependent on the direction of the repair, but generally 30 degrees of rotational stretch is allowed beyond
neutral (external rotation for an anterior repair, internal rotation for a posterior repair), and full rotation is
allowed in the opposite direction. Abduction and elevation are limited for the first 6 weeks to 90 degrees, and
may be limited further for axillary pouch repairs. Muscle
strengthening is timed on the basis of the approach to
the repair. In an all-arthroscopic repair or open repair
which does not take down any muscle, we begin isometric and short chain mobilization and strengthening
immediately to prevent disuse atrophy. In cases where
the subscapularis is taken down anteriorly, resisted
internal rotation is limited until healing of the tendon
is assured, usually around the 8-week point postoperatively. Once tissue healing is assured, patients are placed
in a return-to-sport program that emphasizes dynamic
stabilization with an emphasis on scapular rhythm.
Co-contraction exercises of the anterior and posterior
rotator cuff as well as specific exercises to target the
periscapular musculature are emphasized. If the patient
is an athlete, return to sport may be considered once he
or she regains dynamic strength and rhythm as well as
endurance and confidence.
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152 Section 2 Anterior Instability
S u mmary
Instability due to HAGL lesions can be a diagnostic and therapeutic challenge. Seven types of HAGL
lesions have been reported in the literature, and care
must be taken to ascertain an accurate diagnosis in
order to optimize treatment. When HAGL lesions
occur, trauma, either macro or repetitive, is the usual
cause. Evaluations must include a thorough search for
associated pathology. The diagnostic imaging of choice
is the MR arthrogram with the “J” sign and extravasation along the medial humeral attachment representing the cardinal signs of capsular failure and a HAGL
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